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La Glisodin®, un extrait de melon, atténue l’apoptose des cardiomyocytes via la suppression du stress oxydant cardiaque au cours du diabète chronique expérimental

Glisodin®, a melon extract that attenuates cardiac cell death via suppression of oxidative stress in the heart of Wistar rat with streptozotocin-induced diabetes

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  • Pharmacognosie
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Phytothérapie

Résumé

Nous avons cherché à vérifier si l’atténuation du stress oxydatif lié au diabète pourrait diminuer le processus de la mort des cellules cardiaques. Notre étude a montré que l’apoptose cardiaque est semblable à une des réponses cellulaires majeures au diabète: induite par un stress oxydatif. La Glisodin®, une association de SOD de melon et de protéine de blé, également un puissant antioxydant, a freiné le développement de la cardiomyopathie diabétique. Nos résultats montrent une réduction significative des TUNEL-positifs dans les cardiomyocytes, observée chez le groupe diabétique traité par la Glisodin®. On a observé une diminution significative de la teneur en glutathion réduit, de l’activité de la SOD et de la catalase dans le cœur de rats diabétiques accompagnée par une augmentation des concentrations plasmatiques des LPO en comparaison aux rats traités par Glisodin®. Le traitement des rats diabétiques par la Glisodin® a rétabli l’augmentation de l’activité de la LDH et de la CPK exprimée chez les rats non traités. En conclusion, nos résultats suggèrent que l’atténuation de l’apoptose des cellules cardiaques par la Glisodin® assoie son effet préventif contre le développement de la cardiomyopathie diabétique. Toutefois, cet effet est principalement médié par une action antioxydante suppressive du stress oxydatif plutôt que par une action hypoglycémiante.

Abstract

We aimed to test whether attenuation of cardiac cell death can prevent diabetic cardiomyopathy. Our study showed that cardiac apoptosis as a major cellular response to diabetes is induced by hyperglycemia-derived oxidative stress. Glisodin® as a potent antioxidant prevents the development of diabetic cardiomyopathy. Eight weeks after STZ treatment, cardiac apoptosis was examined by terminal deoxynucleotidyl transferase-mediated dUTP labeling (TUNEL) assay. Oxidative stress in the heart tissue was evaluated by measuring GSH content, LPO level, and catalase and SOD activities. Cardiomyopathy was evaluated by measuring LDH and CPK activities. Our results show a significant reduction in diabetesinduced increases in TUNEL-positive cells was observed in a Glisodin® treatment group. A significant decrease of reduced glutathione content, superoxide dismutase, and catalase activities in the heart of diabetic rats accompanied by increased LPO plasma levels, but not in Glisodin®-treated rats, was observed. LDH and CPK activities as biomarkers of cardiomyopathy were decreased in Glisodin®-treated diabetic rats compared to diabetic-controlled rats. In conclusion, our results suggest that attenuation of cardiac cell death by Glisodin® treatment results in a significant prevention of the development of diabetic cardiomyopathy. This process is mediated by the antioxidant effect of Glisodin® to suppress oxidative stress in the heart.

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Trea, F., Ouali, K., Baba-Ahmed, F. et al. La Glisodin®, un extrait de melon, atténue l’apoptose des cardiomyocytes via la suppression du stress oxydant cardiaque au cours du diabète chronique expérimental. Phytothérapie 11, 339–347 (2013). https://doi.org/10.1007/s10298-013-0818-2

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